Autophagic proteins: New facets of the oxygen paradox

Yang Jin, Akihiko Tanaka, Augustine M.K. Choi, Stefan W. Ryter

Research output: Contribution to journalShort surveypeer-review

29 Scopus citations

Abstract

Oxygen (O2), while essential for aerobic life, can also cause metabolic toxicity through the excess generation of reactive oxygen species (ROS). Pathological changes in ROS production can originate through the partial reduction of O2 during mitochondrial electron transport, as well as from enzymatic sources. This phenomenon, termed the oxygen paradox, has been implicated in aging and disease, and is especially evident in critical care medicine. Whereas high O2 concentrations are utilized as a life-sustaining therapeutic for respiratory insufficiency, they in turn can cause acute lung injury. Alveolar epithelial cells represent a primary target of hyperoxiainduced lung injury. Recent studies have indicated that epithelial cells exposed to high O2 concentrations die by apoptosis, or necrosis, and can also exhibit mixed-phenotypes of cell death (aponecrosis). Autophagy, a cellular homeostatic process responsible for the lysosomal turnover of organelles and proteins, has been implicated as a general response to oxidative stress in cells and tissues. This evolutionarily conserved process is finely regulated by a complex interplay of protein factors. During autophagy, senescent organelles and cellular proteins are sequestered in autophagic vacuoles (autophagosomes) and subsequently targeted to the lysosome, where they are degraded by lysosomal hydrolases, and the breakdown products released for reutilization in anabolic pathways. Autophagy has been implicated as a cell survival mechanism during nutrient-deficiency states, and more generally, as a determinant of cell fate. However, the mechanisms by which autophagy and/or autophagic proteins potentially interact with and/or regulate cell death pathways during high oxygen stress, remain only partially understood.

Original languageEnglish (US)
Pages (from-to)426-428
Number of pages3
JournalAutophagy
Volume8
Issue number3
DOIs
StatePublished - Mar 2012

Keywords

  • Acute lung injury
  • Apoptosis
  • Autophagy
  • Caveolin-1
  • Fas
  • Hyperoxia
  • LC3B

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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